scholarly journals Conditional Essentiality of the csrA Gene in Escherichia coli

2008 ◽  
Vol 191 (5) ◽  
pp. 1722-1724 ◽  
Author(s):  
Johan Timmermans ◽  
Laurence Van Melderen
Keyword(s):  
Escherichia Coli ◽  
Growth Inhibition ◽  
Deletion Mutant ◽  
Glycogen Synthesis ◽  
Synthetic Medium ◽  
Carbon Sources ◽  
Krebs Cycle ◽  
Physiological Processes

ABSTRACT CsrA is a global posttranscriptional regulator of numerous physiological processes, such as glycogenesis and glycolysis. Here, we show that the csrA gene of Escherichia coli is essential for growth on LB and on synthetic medium containing glycolytic carbon sources. However, csrA is not necessary for growth on synthetic medium containing pyruvate, showing that the Krebs cycle is functional in the csrA::cat deletion mutant. Deletion of the glgCAP operon in the csrA::cat mutant restored the ability to grow on LB and on synthetic medium containing glycolytic carbon sources, showing that growth inhibition is due to an excess of glycogen synthesis.

scholarly journals Functional Interactions between the Carbon and Iron Utilization Regulators, Crp and Fur, in Escherichia coli

2005 ◽  
Vol 187 (3) ◽  
pp. 980-990 ◽  
Author(s):  
Zhongge Zhang ◽  
Guillermo Gosset ◽  
Ravi Barabote ◽  
Claudio S. Gonzalez ◽  
William A. Cuevas ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Transcription Factors ◽  
Fatty Acid Synthase ◽  
Glycogen Synthesis ◽  
Krebs Cycle ◽  
Receptor Protein ◽  
Published Data ◽  
Cyclopropane Fatty Acid ◽  
Gene Encoding ◽  
Genes Encoding

ABSTRACT In Escherichia coli, the ferric uptake regulator (Fur) controls expression of the iron regulon in response to iron availability while the cyclic AMP receptor protein (Crp) regulates expression of the carbon regulon in response to carbon availability. We here identify genes subject to significant changes in expression level in response to the loss of both Fur and Crp. Many iron transport genes and several carbon metabolic genes are subject to dual control, being repressed by the loss of Crp and activated by the loss of Fur. However, the sodB gene, encoding superoxide dismutase, and the aceBAK operon, encoding the glyoxalate shunt enzymes, show the opposite responses, being activated by the loss of Crp and repressed by the loss of Fur. Several other genes including the sdhA-D, sucA-D, and fumA genes, encoding key constituents of the Krebs cycle, proved to be repressed by the loss of both transcription factors. Finally, the loss of both Crp and Fur activated a heterogeneous group of genes under σS control encoding, for example, the cyclopropane fatty acid synthase, Cfa, the glycogen synthesis protein, GlgS, the 30S ribosomal protein, S22, and the mechanosensitive channel protein, YggB. Many genes appeared to be regulated by the two transcription factors in an apparently additive fashion, but apparent positive or negative cooperativity characterized several putative Crp/Fur interactions. Relevant published data were evaluated, putative Crp and Fur binding sites were identified, and representative results were confirmed by real-time PCR. Molecular explanations for some, but not all, of these effects are provided.

scholarly journals Effects of Meal Fructose/Glucose Composition on Postprandial Glucose Appearance and Hepatic Glycogen Synthesis in Healthy Subjects

2021 ◽  
Vol 10 (4) ◽  
pp. 596
Author(s):  
Cristina Barosa ◽  
Rogério T. Ribeiro ◽  
Rita Andrade ◽  
João F. Raposo ◽  
John G. Jones
Keyword(s):  
Plasma Glucose ◽  
Healthy Subjects ◽  
Glycogen Synthesis ◽  
Krebs Cycle ◽  
Hepatic Glycogen ◽  
Indirect Pathway ◽  
Metabolic Complications ◽  
Glucose Ratio ◽  
Dietary Fructose ◽  
P Sources

Dietary fructose overshadows glucose in promoting metabolic complications. Intestinal fructose metabolism (IFM) protects against these effects in rodents, by favoring gluconeogenesis, but the extent of IFM in humans is not known. We therefore aimed to infer the extent of IFM by comparing the contribution of dietary fructose to systemic glucose and hepatic glycogen appearance postprandially. Twelve fasting healthy subjects ingested two protein meals in random order, one supplemented with 50 g 5/95 fructose/glucose (LF) and the other with 50 g 55/45 fructose/glucose (HF). Sources of postprandial plasma glucose appearance and hepatic glycogen synthesis were determined with deuterated water. Plasma glucose excursions, as well as pre- and post-meal insulin, c-peptide, and triglyceride levels were nearly identical for both meals. The total gluconeogenic contribution to plasma glucose appearance was significantly higher for HF versus LF (65 ± 2% vs. 34 ± 3%, p < 0.001). For HF, Krebs cycle anaplerosis accounted for two-thirds of total gluconeogenesis (43 ± 2%) with one-third from Triose-P sources (22 ± 1%). With LF, three-quarters of the total gluconeogenic contribution originated via Krebs cycle anaplerosis (26 ± 2%) with one-quarter from Triose-P sources (9 ± 2%). HF and LF gave similar direct and indirect pathway contributions to hepatic glycogen synthesis. Increasing the fructose/glucose ratio had significant effects on glucose appearance sources but no effects on hepatic glycogen synthesis sources, consistent with extensive IFM. The majority of fructose carbons were converted to glucose via the Krebs cycle.

scholarly journals Phage genetic sites involved in lambda growth inhibition by the Escherichia coli rap mutant.

Genetics ◽  
1989 ◽  
Vol 121 (3) ◽  
pp. 401-409
Author(s):  
P Guzmán ◽  
G Guarneros
Keyword(s):  
Escherichia Coli ◽  
Growth Inhibition ◽  
Phage Genome ◽  
Bacteriophage Lambda ◽  
Phage Lambda ◽  
Wild Type ◽  
Attp Site

Abstract The rap mutation of Escherichia coli prevents the growth of bacteriophage lambda. We have isolated phage mutants that compensate for the host deficiency. The mutations, named bar, were genetically located to three different loci of the lambda genome: barI in the attP site, barII in the cIII ea10 region, and barIII within or very near the imm434 region. The level of lambda leftward transcription correlates with rap exclusion. Phage lambda mutants partially defective in the pL promoter or in pL-transcript antitermination showed a Bar- phenotype. Conversely, mutants constitutive for transcription from the pI or pL promoters were excluded more stringently by rap bacteria. We conclude that rap exclusion depends on the magnitude of transcription through the wild type bar loci in the phage genome.

scholarly journals The growth of Paracoccus halodenitrificans in a defined medium

1984 ◽  
Vol 30 (6) ◽  
pp. 837-840 ◽  
Author(s):  
Lawrence I. Hochstein ◽  
Geraldine A. Tomlinson
Keyword(s):  
Synthetic Medium ◽  
Carbon Sources ◽  
Defined Medium ◽  
Anaerobic Growth ◽  
Inorganic Salts ◽  
Vitamin B ◽  
Aerobic Growth ◽  
Methionine Biosynthesis ◽  
Dependent Pathway

A synthetic medium, consisting of inorganic salts and any of a number of carbon sources, supported the aerobic growth of Paracoccus halodenitrificans when supplemented with thiamine. The same medium plus an appropriate nitrogenous oxide supported anaerobic growth when additionally supplemented with methionine. The observation that vitamin B12 or betaine replaced methionine suggested that P. halodenitrificans had a defect in the cobalamin-dependent pathway for methionine biosynthesis, as well as the inability to synthesize betaine when growing anaerobically.

scholarly journals The Maltodextrin System of Escherichia coli: Metabolism and Transport

2005 ◽  
Vol 187 (24) ◽  
pp. 8322-8331 ◽  
Author(s):  
Renate Dippel ◽  
Winfried Boos
Keyword(s):  
Escherichia Coli ◽  
Abc Transporter ◽  
Binding Protein ◽  
Glycogen Synthesis ◽  
Equilibrium Conditions ◽  
Per Se ◽  
Maltodextrin Phosphorylase ◽  
Internal Level

ABSTRACT The maltose/maltodextrin regulon of Escherichia coli consists of 10 genes which encode a binding protein-dependent ABC transporter and four enzymes acting on maltodextrins. All mal genes are controlled by MalT, a transcriptional activator that is exclusively activated by maltotriose. By the action of amylomaltase, we prepared uniformly labeled [14C]maltodextrins from maltose up to maltoheptaose with identical specific radioactivities with respect to their glucosyl residues, which made it possible to quantitatively follow the rate of transport for each maltodextrin. Isogenic malQ mutants lacking maltodextrin phosphorylase (MalP) or maltodextrin glucosidase (MalZ) or both were constructed. The resulting in vivo pattern of maltodextrin metabolism was determined by analyzing accumulated [14C]maltodextrins. MalP− MalZ+ strains degraded all dextrins to maltose, whereas MalP+ MalZ− strains degraded them to maltotriose. The labeled dextrins were used to measure the rate of transport in the absence of cytoplasmic metabolism. Irrespective of the length of the dextrin, the rates of transport at a submicromolar concentration were similar for the maltodextrins when the rate was calculated per glucosyl residue, suggesting a novel mode for substrate translocation. Strains lacking MalQ and maltose transacetylase were tested for their ability to accumulate maltose. At 1.8 nM external maltose, the ratio of internal to external maltose concentration under equilibrium conditions reached 106 to 1 but declined at higher external maltose concentrations. The maximal internal level of maltose at increasing external maltose concentrations was around 100 mM. A strain lacking malQ, malP, and malZ as well as glycogen synthesis and in which maltodextrins are not chemically altered could be induced by external maltose as well as by all other maltodextrins, demonstrating the role of transport per se for induction.

scholarly journals Genetic variation in the dietary sucrose modulation of enzyme activities in Drosophila melanogaster

1984 ◽  
Vol 43 (3) ◽  
pp. 307-321 ◽  
Author(s):  
Billy W. Geer ◽  
Cathy C. Laurie-Ahlberg
Keyword(s):  
Drosophila Melanogaster ◽  
Genetic Variation ◽  
Enzyme Activities ◽  
Glycogen Synthesis ◽  
Krebs Cycle ◽  
Natural Populations ◽  
Substitution Lines ◽  
Chromosome Substitution Lines ◽  
High Sucrose Diet ◽  
Selection Of

SUMMARYGenetic variation in the modulating effect of dietary sucrose was assessed in Drosophila melanogaster by examining 27 chromosome substitution lines coisogenic for the X and second chromosomes and possessing different third isogenic chromosomes derived from natural populations. An increase in the concentration of sucrose from 0·1% to 5% in modified Sang's medium C significantly altered the activities of 11 of 15 enzyme activities in third instar larvae, indicating that dietary sucrose modulates many, but not all, of the enzymes of D. melanogaster. A high sucrose diet promoted high activities of enzymes associated with lipid and glycogen synthesis and low activities of enzymes of the glycolytic and Krebs cycle pathways, reflecting the physiological requirements of the animal. Analyses of variance revealed significant genetic variation in the degrees to which sucrose modulated several enzyme activities. Analysis of correlations revealed some relationships between enzymes in the genetic effects on the modulation process. These observations suggest that adaptive evolutionary change may depend in part on the selection of enzyme activity modifiers that are distributed throughout the genome.

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